Overexpression of MAC30 is associated with poor clinical outcome in human non-small-cell lung cancer.

The aim of this study was to detect MAC30 expression in human non-small cell lung cancer (NSCLC) and to analyze its association with prognosis of NSCLC patients. Quantitative real-time RT-PCR was performed to examine the expression of MAC30 mRNA in 20 cases of NSCLC and corresponding non-tumor tissue samples. Immunohistochemistry was performed to detect the expression of MAC30 in 95 NSCLC tissues. We found that the expression levels of MAC30 mRNA in NSCLC tissues were significantly higher than those in corresponding non-tumor tissues. High-level MAC30 expression was correlated with poor tumor differentiation, TNM stage, and lymph node metastasis. Patients with high expression levels of MAC30 showed lower overall survival rate than those with low expression levels. Multivariate analysis showed that high MAC30 protein expression was an independent prognostic factor for NSCLC patients. Our study suggests that over-expression of MAC30 may play an important role in the progression of NSCLC and MAC30 expression may offer a valuable marker for predicting the outcome of patients with NSCLC.

[Effects of emodin on proliferation cycle and apoptotic gene of human lung adenocarcinoma cell line Anip 973].

OBJECTIVE: To study the suppressive role of emodin on the growth and its effect on the proliferation cycle and apoptotic gene of human lung adenocarcinoma cell line Anip 973. METHODS: The survival rate and the inhibitory rate of Anip 973 cell in vitro were detected by MTT colorimetric assay and cell growth curve assay at different time points under different concentration of emodin; the cell proliferation cycle and the apoptotic rate were examined with flow cytometry analysis, and Caspase-3 protein expression was measured by immunoblotting assay. RESULTS: Emodin inhibited the proliferation of Anip 973 cell at G0/G1 phase, decreased the cell ratio at S phase and activated the Caspase-3 protein. It suppressed the growth of tumor cells and raised the apoptotic rate in a concentration and time depending manner in a certain extent. CONCLUSION: Emodin could suppress the proliferation of Anip 973 cell, and its mechanism of anticancer effect may be through activating Caspase-3, to induce apoptosis and block cell cycle.

DNA microarray reveals different pathways responding to paclitaxel and docetaxel in non-small cell lung cancer cell line.

The wide use of paclitaxel and docetaxel in NSCLC clinical treatment makes it necessary to find biomarkers for identifying patients who can benefit from paclitaxel or docetaxel. In present study, NCI-H460, a NSCLC cell line with different sensitivity to paclitaxel and docetaxel, was applied to DNA microarray expression profiling analysis at different time points of lower dose treatment with paclitaxel or docetaxel. And the complex signaling pathways regulating the drug response were identified, and several novel sensitivity-realted markers were biocomputated.The dynamic changes of responding genes showed that paclitaxel effect is acute but that of docetaxel is durable at least for 48 hours in NCI-H460 cells. Functional annotation of the genes with altered expression showed that genes/pathways responding to these two drugs were dramatically different. Gene expression changes induced by paclitaxel treatment were mainly enriched in actin cytoskeleton (ACTC1, MYL2 and MYH2), tyrosine-protein kinases (ERRB4, KIT and TIE1) and focal adhesion pathway (MYL2, IGF1 and FLT1), while the expression alterations responding to docetaxel were highly co-related to cell surface receptor linked signal transduction (SHH, DRD5 and ADM2), cytokine-cytokine receptor interaction (IL1A and IL6) and cell cycle regulation (CCNB1, CCNE2 and PCNA). Moreover, we also confirmed some different expression patterns with real time PCR. Our study will provide the potential biomarkers for paclitaxel and docetaxel-selection therapy in clinical application.